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STUDYING THE ANTI-INFLAMMATORY PROPERTIES OF
CERTAIN MEDICINAL PLANTS
Nabiyev Jasurbek Qosimjon o‘g‘li
Andijon davlat universiteti
Maqola haqida ma’lumot
Qabul qilingan: 04.07.2024
Qayta qabul: 10.07.2024
Saytda mavjud: 18.06.2024
Muallif (lar)
N.Q.Nabiyev
10.69891/3060-4540.2024.4.1.001
https://doi.org/10.5281/zenodo.12772933
https://scholar.google.com/scholar?hl=ru&as_sdt=0%2C5&
Muallif bilan aloqa
https://orcid.org/0009-0002-0641-2623
© N.Q.Nabiyev
UNIVERSAL xalqaro ilmiy jurnal
Ochiq ma’lumotlar:
https://universaljurnal.uz/index.php/jurnal
Maxfiylik bayonoti
Materialni istalgan vosita yoki formatda nusxalash va qayta
tarqatish hamda maqoladan toʻgʻri iqtibos keltirish va
litsenziyasini koʻrsatish sharti bilan istalgan maqsadda
foydalanish mumkin.
Annotation:
Nowadays, new types of inflammation
are emerging. Each of them is related to the activity of
individual organs and organ systems. In general, all
diseases are actually "Inflammation." Their development
varies depending on acute and chronic conditions. This
article presents information about their molecular
mechanisms and some of the plants used in folk medicine
to combat them.
Keywords.
Inflammation, molecular mechanism,
chemical
composition,
cyclooxygenase
(COX),
Prostaglandins, Rosa L, Sinapis arvensis, Amygdalus
communis L.
Аннотация:
В настоящее время появляются новые
виды воспалений. Каждый из них связан с
деятельностью отдельных органов и систем органов.
В общем, все болезни на самом деле являются
«воспалениями».
Их
развитие
варьирует
в
зависимости от острых и хронических состояний. В
данной статье представлена информация об их
молекулярных механизмах и некоторых растениях,
используемых в народной медицине для борьбы с
ними.
Ключевые слова.
Воспаление, молекулярный
механизм, химический состав, циклооксигеназа
(ЦОГ), простагландины, Rosa L, Sinapis arvensis,
Amygdalus communis L.
Hozirgi vaqtda yallig'lanishning
yangi turlari paydo bo'lmoqda. Ularning har biri alohida
organlar va organ tizimlarining faoliyati bilan bog'liq.
Umuman olganda, barcha kasalliklar aslida "yallig'lanish"
dir. Ularning rivojlanishi o'tkir va surunkali holatlarga
qarab farq qiladi. Ushbu maqolada ularning molekulyar
mexanizmlari va ularga qarshi kurashish uchun xalq
tabobatida qo'llaniladigan ba'zi o'simliklar haqida
ma'lumot berilgan.
Kalit so‘zlar.
Yallig'lanish, molekulyar mexanizm,
kimyoviy
tarkibi,
siklooksigenaza
(COX),
Prostaglandinlar, Rosa L, Sinapis arvensis, Amygdalus
communis L.
Universal International Scientific Journal
Universal Xalqaro Ilmiy Jurnal
Jurnalning bosh sahifasi:
Universal International Scientific Journal
46
UNIVERSAL international scientific journal
Inflammation is often a complex process
associated with pain, involving phenomena such
as increased vascular permeability, enhanced
protein denaturation, and membrane changes.
When div cells are damaged by microbes,
physical factors, or chemical agents, the damage
manifests as stress. Tissue inflammation occurs
as a response to stress, characterized by redness,
pain, heat, swelling, and loss of function in the
affected area. Loss of function depends on the
location and extent of the damage. Since
inflammation is one of the div's non-specific
defense mechanisms, the reaction of randomly
cut tissues is similar to other types of tissue
damage caused by heat, radiation, bacterial, or
viral invasion. Prostaglandins are hormone-like
substances synthesized in almost all tissues of
the div, including blood vessel walls. They
regulate blood pressure, uterine contractions,
and various other physiological processes.
Prostaglandins
are
small
molecules
belonging to a group of lipid-like substances
called eicosanoids. This group also includes
chemically
similar
compounds
like
leukotrienes, involved in inflammation and
allergic reactions, and thromboxanes, involved
in blood clotting. All eicosanoids are derived
from arachidonic acid, an unsaturated fatty acid,
and are synthesized from another fatty acid,
linolenic acid, which enters the human div
with food.
Molecular Mechanisms of
Inflammation
Cyclooxygenases (COX) are enzymes
involved in synthesizing prostanoids such as
prostaglandins,
prostacyclins,
and
thromboxanes. Pharmacological inhibition of
cyclooxygenases reduces inflammation and
pain, with aspirin and ibuprofen being examples
of such inhibitors. The terms "prostaglandin
synthase" and "prostaglandin synthetase"
are
sometimes
used
to
refer
to
cyclooxygenases. Detailed studies of COX
revealed their presence in various tissues
and their different sensitivity spectra to
aspirin-like drugs, suggesting the existence
of enzyme isoforms. In humans, two genes
encode COX: COX-1 and COX-2. The
alternative splicing of the first gene's
product results in two forms of the enzyme.
Cyclooxygenases catalyze the conversion
of arachidonic acid to prostaglandin H2
(PGH2),
a
precursor
of
other
prostaglandins,
prostacyclins,
and
thromboxane A2.**Inflammation is one of
the central processes required to protect
animal cells from injuries or microbial
infections
[1,2].
Nevertheless,
inflammation is regularly acute [3] or
chronic [1]. Chronic inflammation leads to
various
diseases,
including
neurodegenerative disorders, cancer, and
cardiovascular
diseases
[4].
The
inflammation mechanism represents a
chain of coordinated, dynamic responses,
including specific humoral secretions with
cellular and vascular events. These
pathways involve the physical alteration of
white blood cell locations (monocytes,
basophils, eosinophils, and neutrophils),
plasma, and fluids to the inflamed site [5].
A group of latent mediators and other
signaling molecules (such as histamine,
prostaglandins, leukotrienes, oxygen and
nitrogen-derived
free
radicals,
and
serotonin) is primarily released by immune
defense
cells
in
the
inflammatory
mechanism
[6].
Regardless,
the
inflammatory response is triggered in two
stages: (a) acute and (b) chronic, each
Universal International Scientific Journal
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UNIVERSAL international scientific journal
mediated by different mechanisms [3]. The
acute inflammation involves the participation of
immune responses vascular and cellular [7].
Responses occurring in microvasculature
typically emerge within minutes of tissue injury
or microbial infection, involving inflammatory
stimuli known as vascular events [7]. This
process quickly leads to vasodilation and
subsequently
makes
the
vessels
more
permeable. These processes allow the entry of
inflammatory mediators and produce interstitial
edema [8]. During inflammation, the infiltration
of white blood cells from the circulatory system
is crucial [9,10]. A group of chemotactic agents,
such as microbial endotoxins with amino-
terminal N-formyl methionyl groups, C5a
complement fragments, and interleukins, along
with platelet-activating factors like histamine
and leukotriene B, can stimulate leukocytes to
swim
within
minutes
[11,12].
Among
leukocytes,
neutrophils
are
the
first
inflammatory cells recruited to the acute
inflammation site [13]. The infiltration of
immune cells is triggered by a complex
mechanism where white blood cells work
together with endothelial cells in post-capillary
venules [14]. The cellular events encompass a
sequence involving capture, trundling, and
adhesion to microvascular endothelium [15].
These events are regulated by the mobilization
of cell adhesion molecules (CAMs). These
CAMs include intracellular adhesion molecules
(ICAM)-1, ICAM-2, integrins, and selectins.
The selectin group of CAMs includes three
families: P-selectin and E-selectin produced by
endothelial cells and L-selectin produced by
white blood cells [16]. High-affinity binding
between integrins (CD11/CD18) and adhesion
molecules (CAM-1 and CAM-2) on white blood
cells and endothelial cells mediates the adhesion
of white blood cells to endothelium [17].
After the stationary adhesion period, white
blood cells can exit post-capillary venules
by
extending
pseudopodia
between
endothelial
cells
and
reaching
the
subendothelial space. This complex event
is
often
called
white
blood
cell
extravasation
and
transendothelial
migration [18]. Chronic inflammatory
events are characterized by mononuclear
cell infiltration (such as monocytes and
lymphocytes),
fibroblast
proliferation,
collagen fibers, and connective tissue
formation,
eventually
leading
to
granuloma
formation
[19].
The
degeneration
of
tissues
in
chronic
inflammation is usually mediated by
nitrogen species, proteases, and other
reactive oxygen species released by
infiltrated inflammatory cells [20]. Indeed,
genomic changes in p53 have been
confirmed as a cause of most chronic
inflammatory
diseases
(such
as
inflammatory
bowel
disease
and
rheumatoid arthritis) and cancer [21-23].
The novelty of this review is that it
provides a summary of recent knowledge
on the involvement of mediators in
inflammation
and
addresses
some
misconceptions
and
facts
about
inflammatory processes. This review aims
to highlight the knowledge gap about
inflammation processes, including the
addition of the latest and most relevant
issues concerning this phenomenon.
Inflammation is a crucial mechanism
for human health and disease. The first
description of inflammation by Roman
Cornelius Celsus in the 1st century
identified
the
clinical
signs
of
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UNIVERSAL international scientific journal
inflammatory diseases. Four main signs of
inflammation were identified: rubor et tumor
cum calore et dolore (redness and heat with
swelling and pain). The development of the
disease was defined by these four cardinal signs
[24,25]. In 1858, the inclusion of an additional
cardinal sign, functio laesa (loss of function),
was proposed by Rudolf Virchow's study of the
cellular basis of pathology. Subsequent research
in the late 19th century included the microbial
theory of disease, with microorganisms
identified as the primary inducers of the acute
inflammatory response by Robert Koch and
Louis Pasteur. Metchnikoff discovered that
acute
inflammation
is
resolved
when
neutrophils are engulfed by tissue macrophages.
Recently, advanced cellular and molecular
mechanisms
controlling
the
fate
of
inflammation have been identified. Acute
inflammation is considered a physiological
response to protect vascularized tissues and
maintain homeostasis. Inflammation begins as a
protective response to problems related to
pathogens or foreign bodies or injuries
experienced by host tissues. This process is
characterized by blood vessel dilation, increased
capillary permeability, enhanced blood flow,
and the recruitment of leukocytes. Among the
first leukocytes to accumulate at the inflamed
site are polymorphonuclear neutrophils. These
cells are crucial as the first line of defense for
the innate immune system due to their
phagocytic
and
microbicidal
functions.
Subsequently, mononuclear cells, monocytes,
and macrophages enter the inflammatory site
and clear cellular debris and apoptotic
polymorphonuclear
neutrophils
through
nonphlogistic (non-heat or fever-producing)
phagocytosis, avoiding the extension of
inflammation [26].
While the inflammatory reaction is
protective, the failure to clear harmful
materials produced by neutrophils through
phagocytosis,
the
non-clearance
of
apoptotic inflammatory cells, and the delay
of apoptosis lead to chronic and
pathological lesions. Complete removal of
leukocytes from the lesion is observed in
sensitive individuals; acute inflammation
is not resolved and chronic disease and
fibrosis develop [27]. Accordingly, the
failure to resolve and restore tissue
homeostasis through neutrophil-mediated
clearance leads to chronic inflammation
[28]. This is a primary cause of human
inflammatory
pathologies,
including
arthritis, asthma, cancer, cardiovascular
diseases, and periodontal diseases. From
the time of Celsus, we have thought about
inflammation in terms of induction. In
recent years, we have identified the
molecular mediators of inflammation
induction (cytokines and chemokines) as
our understanding of the process at the
molecular level has evolved. We have
never paid attention to attenuation; how is
inflammation turned off? We have always
assumed this was a passive process due to
the cessation or breakdown of inducers. To
maintain a healthy state, both the initiation
and resolution of acute inflammation must
be effective. The loss of resolution and the
failure to restore tissue homeostasis due to
neutrophil-mediated clearance leads to
chronic inflammation [28]. This is a
primary cause of human inflammatory
pathologies, including arthritis, asthma,
cancer,
cardiovascular
diseases,
and
periodontal diseases. From the time of
Celsus,
we
have
thought
about
Universal International Scientific Journal
49
UNIVERSAL international scientific journal
inflammation in terms of induction. In recent
years, we have identified the molecular
mediators of inflammation induction (cytokines
and chemokines) as our understanding of the
process at the molecular level has evolved. We
have never paid attention to attenuation; how is
inflammation turned off? We have always
assumed this was a passive process due to the
cessation or breakdown of inducers. To
maintain a healthy state, both the initiation and
resolution of acute inflammation must be
effective. The loss of resolution and the failure
to
restore
tissue
homeostasis
through
neutrophil-mediated clearance lead to chronic
inflammation [28]. This is a primary cause of
human inflammatory pathologies, including
arthritis,
asthma,
cancer,
cardiovascular
diseases, and periodontal diseases. From the
time of Celsus, we have thought about
inflammation in terms of induction. In recent
years, we have identified the molecular
mediators of inflammation induction (cytokines
and chemokines) as our understanding of the
process at the molecular level has evolved. We
have never paid attention to attenuation; how is
inflammation turned off? We have always
assumed this was a passive process due to the
cessation or breakdown of inducers. To
maintain a healthy state, both the initiation and
resolution of acute inflammation must be
effective. The loss of resolution and the failure
to
restore
tissue
homeostasis
through
neutrophil-mediated clearance lead to chronic
inflammation [28]. This is a primary cause of
human inflammatory pathologies, including
arthritis,
asthma,
cancer,
cardiovascular
diseases, and periodontal diseases. From the
time of Celsus, we have thought about
inflammation in terms of induction. In recent
years, we have identified the molecular
mediators of inflammation induction
(cytokines and chemokines) as our
understanding of the process at the
molecular level has evolved. We have
never paid attention to attenuation; how is
inflammation turned off? We have always
assumed this was a passive process due to
the cessation or breakdown of inducers. To
maintain a healthy state, both the initiation
and resolution of acute inflammation must
be effective. The loss of resolution and the
failure to restore tissue homeostasis
through neutrophil-mediated clearance
lead to chronic inflammation [28]. This is
a primary cause of human inflammatory
pathologies, including arthritis, asthma,
cancer,
cardiovascular
diseases,
and
periodontal diseases. From the time of
Celsus,
we
have
thought
about
inflammation in terms of induction. In
recent years, we have identified the
molecular mediators of inflammation
induction (cytokines and chemokines) as
our understanding of the process at the
molecular level has evolved. We have
never paid attention to attenuation; how is
inflammation turned off? We have always
assumed this was a passive process due to
the cessation or breakdown of inducers. To
maintain a healthy state, both the initiation
and resolution of acute inflammation must
be effective. The loss of resolution and the
failure to restore tissue homeostasis
through neutrophil-mediated clearance
lead to chronic inflammation [28]. This is
a primary cause of human inflammatory
pathologies, including arthritis, asthma,
cancer,
cardiovascular
diseases,
and
periodontal diseases.
Universal International Scientific Journal
50
UNIVERSAL international scientific journal
Studying Anti-Inflammatory Properties of
Plants:
1. Take 5 ml of blood and wash it three
times with a 1:1 ratio of saline solution. Prepare
the final blood clot using saline solution at a
10% concentration.
2. Prepare 1 ml of the extract under study
at various concentrations (1000, 800, 600, 400,
and 200 μg/ml) and dissolve it in distilled water
(it should also be soluble in DMSO). Aspirin is
used as a positive control.
3. Add 1 ml of the extract to the test tube,
add 1 ml of the 10% blood solution, and
incubate the mixture in a water bath at 56°C for
30 minutes. Then cool to room temperature.
Centrifuge the mixture at 2500 rpm for 5
minutes, and measure the optical density of the
supernatant
at
560
nm
using
a
spectrophotocolorimeter (the solvent itself is
used as a control).
Results of Studied Plants:
| Local Name | Scientific Name |
Extract Source | Biomass Obtained (gr) |
Extract Obtained (mg) | Anti-Inflammatory
Activity (%) |
|------------------|-----------------------|---------------------|-
----------------------|-----------------------|----------------------------
----|
| Ordinary Reed | Typha orientalis | Leaf |
5.15 | 50 | 87 |
| Ordinary Pigweed | Chenopodium vulgaris | Leaf,
Seed, Stem | 13.8 | 320 | 80 |
| Dandelion | Dandelion officinalis | Leaf, Seed,
Flower | 13.13 | 60 | 96 |
| Peppermint | Mentha piperita | Flower |
20.86 | 840 | 0 |
| American Bugle | Lycopus virginicus | Leaf, Stem
| 20.87 | 840 | 7.03 |
| Field Bindweed | Convolvulus L. | Leaf, Stem
| 5.3 | 250 | 86 |
| Common Blackberry| Caesius L. | Leaf, Stem
| 5.09 | 370 | 86 |
Rosa L (common rosehip):
The fruit
contains up to 4-6%, sometimes up to 15%
vitamin C, vitamins B2, P, E, and K, 12-27
mg% carotene, up to 29% organic acids
(citric, malic, etc.), up to 18% sugars, up to
3.7% pectin, and up to 4.5% tannins. The
seeds and other parts contain active
compounds.
The
fruit
is
rich
in
multivitamins and is used as a natural food
concentrate to treat vitamin deficiency
diseases. High-vitamin varieties (Begger
and Fedchenko rosehips) are used to treat
and prevent vitamin deficiency diseases.
The oil extracted from the seeds and the
oily extract from the fruit pulp are used to
treat burns, trophic ulcers, eczema, skin
diseases, ultraviolet burns, and ulcerative
colitis.
**Sinapis arvensis (wild mustard):**
The seeds contain the glycoside sinigrin
(up to 15% in powder form). Sinigrin is
broken down into glucose, potassium
bisulfate, and allyl isothiocyanate (mustard
essential oil) by the enzyme myrosinase.
Mustard essential oil can be obtained from
fermented seeds through steam distillation.
The seeds contain 1.17-2.89% essential oil,
composed of 40% allyl mustard oil, 50%
crotonyl mustard oil, and trace amounts of
dimethyl sulfide, carbon disulfide, and
other compounds. The seeds also contain
23-47% oil and up to 26% protein. Mustard
preparations are used for inflammatory
diseases,
myositis,
bronchitis,
and
rheumatic diseases.
Amygdalus communis L (common
almond):
Both types of almond seeds
contain 20-60% oil. They contain the
enzyme emulsin (β-glucosidase) and 3% of
the cyanogenic glycoside amygdalin. The
oil is used as a solvent for drugs. The
Universal International Scientific Journal
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residue from the oil extraction is used to obtain
bitter almond water. Sweet almond residue is
used in cosmetics. Bitter almond seeds are toxic,
and consuming 5-10 seeds can be fatal for
children. Bitter almond water is prepared by
hydrolyzing the residue in warm water for
several hours. Sweet almond kernels contain oil
(up to 40-60%), proteins (about 30%),
mucilage, vitamins, pigments, carotenoids,
lycopene, and traces of essential oil (0.5-0.8%),
which gives them their distinctive almond scent.
The oil contains oleic (80%) and linoleic
(15%) acid glycerides. Sweet almond oil
from dehulled seeds contains small
amounts of linolenic and myristic acids,
absent in oil from hulled seeds. Wild bitter
almonds are toxic due to amygdalin, which
releases hydrocyanic acid, benzaldehyde,
and glucose upon hydrolysis. Whole bitter
almonds are odorless but release a
characteristic almond scent when sliced
due to benzaldehyde.
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